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Eph/ephrin interactions modulate vascular sympathetic innervation.

Deborah H Damon1, Jaclyn A teRiele, Stephen B Marko

  • 1Department of Pharmacology, University of Vermont, 89 Beaumont Avenue, Burlington, VT 05405, United States. Deborah.Damon@uvm.edu

Autonomic Neuroscience : Basic & Clinical
|July 20, 2010
PubMed
Summary

Eph/ephrin interactions influence vascular sympathetic nerve growth and function. EphA4 specifically reduced artery reinnervation and increased norepinephrine release, highlighting their role in vascular innervation.

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Published on: September 11, 2018

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Eph and ephrin proteins are crucial for axon guidance and neuronal function.
  • Their role in vascular sympathetic innervation remains largely unexplored.

Purpose of the Study:

  • To investigate the role of eph/ephrin interactions in the growth and function of vascular sympathetic innervation.
  • To determine if eph/ephrin signaling affects sympathetic nerve regeneration and neurotransmitter release in blood vessels.

Main Methods:

  • RT-PCR analysis of eph and ephrin expression in rat sympathetic ganglia and arteries.
  • In vitro binding assays using dissociated sympathetic neurons.
  • Assessment of femoral artery reinnervation in the presence of ephA4-Fc or IgG-Fc.
  • Measurement of norepinephrine release from isolated tail arteries.

Main Results:

  • Both eph and ephrin families (A and B) are expressed in sympathetic neurons and vascular tissues.
  • EphA4 significantly inhibited the reinnervation of denervated femoral arteries.
  • EphA4 enhanced basal norepinephrine release from sympathetic nerve terminals in tail arteries.

Conclusions:

  • Eph/ephrin interactions play a significant role in modulating the growth of vascular sympathetic innervation.
  • EphA4 acts as an inhibitor of sympathetic nerve regeneration in arteries.
  • Eph/ephrin signaling impacts the functional activity of vascular sympathetic nerves, affecting neurotransmitter release.